促炎细胞因子
牙周炎
兰克尔
骨吸收
下调和上调
信号转导
炎症
小干扰RNA
NF-κB
牙槽
化学
医学
牙科
免疫学
细胞生物学
转染
生物
内科学
生物化学
受体
激活剂(遗传学)
基因
作者
Wei Wei,Jiaxin Li,Xinran Liu,Wei Pan,Min Wang,Jinle Li,Yuan Yue,Liang Hao
标识
DOI:10.1016/j.joen.2022.07.009
摘要
Periapical periodontitis develops due to the interplay between root canal microorganisms and host defenses. The mechanism underlying the pathogenesis of periapical periodontitis remains unclear. Regulator of G protein signaling protein 10 (RGS10) has been suggested to play a role in regulating inflammation. This study explored the potential regulatory effects of RGS10 on periapical periodontitis and the proinflammatory pathway of nuclear factor (NF)-κB.Disease models of periapical inflammation in mice were established, and adenovirus-associated virus (AAV) was used to inhibit RGS10 expression. Periapical lesions were detected using micro-computed tomography. Quantitative reverse transcriptase PCR (qRT-PCR), western blotting (WB), enzyme-linked immunosorbent assay (ELISA), enzyme activity staining of tartrate-resistant acid phosphatase, and immunohistochemistry were conducted to assess the role of RGS10 expression on NF-κB proinflammatory signaling, OPG, RANKL, and osteoclasts in the periapical regions of each group. TNFα was used to stimulate L929 cells alone or with small interfering RNA (siRNA). To assess the expression of associated molecules, WB, immunofluorescence, qRT-PCR, and ELISA were performed.RGS10 inhibition increased alveolar bone destruction in periapical periodontitis lesions and substantially enhanced the NF-κB proinflammatory signaling pathway activation level. Furthermore, RGS10 inhibition upregulated the ratio of OPG/RANKL and the maturation of osteoclasts during alveolar bone resorption. L929 cell TNFα stimulation and siRNA transfection confirmed these in vivo results.RGS10 negatively regulates NF-κB proinflammatory signaling in periapical periodontitis and participates in bone remodeling. Therefore, RGS10 is a promising treatment option for long-term chronic periapical inflammation and may be a new target for the artificial regulation of inflammation.
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